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Management of ascites in patients with liver disease

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Ascites is a distressing symptom and is often indicative of decompensated liver cirrhosis, so it requires careful management and empathetic care. This article comes with a self-assessment enabling you to test your knowledge after reading it



Ascites is a distressing symptom that requires demanding treatments, such as taking diuretics, reducing dietary salt or fluid intake, and draining ascitic fluid out of the abdomen (paracentesis). It is also often a sign that liver cirrhosis has progressed from a stable to a decompensated state – and patients with decompensated liver cirrhosis have a poor prognosis. Nurses in advanced roles deal with many aspects of ascites management, from eliciting patient consent and prescribing albumin to performing paracentesis and monitoring electrolytes. This article offers an overview of ascites, its causes, diagnosis, complications and management, with a focus on ascites due to liver cirrhosis.

Citation: Mortimore G (2018) Management of ascites in patients with liver disease. Nursing Times [online]; 114: 10, 36-40.

Author: Gerri Mortimore is non-medical prescriber, registered nurse teacher and senior lecturer in nursing, University of Derby.


Ascites is an abnormal accumulation of fluid in the abdomen, which can vary from small amounts to many litres. It can be graded from 1 to 3 according to the severity of symptoms (Box 1). This article discusses the pathophysiology, diagnosis and management of ascites, as well as implications for nursing practice. Ascites can have many causes, but this article focuses on ascites caused by liver cirrhosis.


Box 1. Grading of ascites

  • Grade 1: mild – only detectable by ultrasound examination
  • Grade 2: moderate – moderate abdominal distension
  • Grade 3: large – marked abdominal distension

Source: Moore and Aithal (2006)


Liver cirrhosis

There are many causes of ascites, such as widespread cancer or heart failure (Table 1), but the most common is cirrhosis of the liver (European Association for the Study of the Liver, 2010). Liver cirrhosis denotes irreversible scarring or fibrosis in the liver due to long-term inflammation and injury. The three most common causes of liver cirrhosis (Box 2) are:


  • Alcohol misuse;
  • Chronic viral hepatitis due to blood-borne viruses such as hepatitis B and C;
  • Non-alcoholic fatty liver disease (NAFLD).

Often, patients with liver disease develop peripheral oedema as well as ascites.


The presence of ascites indicates that cirrhosis has changed from stable (or compensated) cirrhosis to decompensated cirrhosis. Patients with decompensated cirrhosis are at increased risk of serious ill health and have a poor prognosis (Tsochatzis et al, 2014; Tandon and Garcia-Tsao, 2008): the approximate death rate from the time of diagnosis is 40% at one year and 50% at two years (EASL, 2010). In decompensated alcohol-related liver disease, the death rate is around 10-20% at one month from the time of diagnosis (McPherson et al, 2016). Patients diagnosed with cirrhotic ascites should be referred for liver transplant assessment where appropriate.


Table 1. Causes of ascites

Table 1. Causes of ascites

Box 2. Some causes of liver cirrhosis

  • Alcohol misuse
  • Chronic viral hepatitis B
  • Chronic viral hepatitis C
  • Non-alcoholic fatty liver disease
  • Autoimmune diseases:
    • Autoimmune hepatitis
    • Primary biliary cholangitis
    • Primary sclerosing cholangitis
  • Genetic diseases:
    • Haemochromatosis
    • Alpha 1 antitrypsin deficiency
    • Wilson’s disease

Portal hypertension

With every heartbeat, blood is pumped around the body and enters the liver via the portal vein, which carries blood from the stomach, pancreas, spleen and intestines to the liver through the capillary-like hepatic sinusoids. In cirrhosis, the normal architecture of the liver is replaced by scar tissue, so not all the blood can enter the organ. This results in back pressure, which leads to portal hypertension – an increase in blood pressure (BP) within the portal venous system (Kumar and Clark, 2017). Ascites is one of three life-threatening complications of portal hypertension, the other two being varices and hepatic encephalopathy (Box 3).


Box 3. Portal hypertension: life-threatening complications

Life-threatening complications of portal hypertension include:

  • Ascites
  • Hepatic encephalopathy
  • Varices:
    • Stomach
    • Oesophagus
    • Rectal
    • Umbilical

Varices form in the stomach, oesophagus, umbilicus and rectum due to the high portal venous pressure; as these varices contain blood under extremely high pressure, they can rupture. If not treated quickly, the ensuing catastrophic bleed can lead to death.


Hepatic encephalopathy is characterised by a decline in brain function ranging from vague memory loss and confusion to coma. Again, if not treated quickly, it can lead to death.


Patients presenting with any of these complications of portal hypertension, with or without jaundice, are described as having decompensated liver cirrhosis.


Formation of ascites

Portal hypertension causes the formation of shunts, which bypass the liver and connect the portal venous system to the systemic circulation. Substances such as nitric oxide, prostaglandins and atrial natriuretic peptide (a cardiac hormone that helps to lower BP), which are normally ‘mopped up’ and/or broken down by the liver, are therefore released into the systemic circulation (Kumar and Clark, 2017).


These substances cause arteries to dilate, which in turn causes BP to fall. A vicious cycle ensues: the fall in BP causes the kidneys to retain salt and water, making it even more difficult for the body to rid itself of ascites. Furthermore, the dilation of blood vessels increases the risk of lymph leakage, which leads to the formation of ascites.


As cirrhosis progresses, the liver is unable to produce enough of the protein albumin, so albumin levels fall. One of the functions of albumin is to help hold fluid within cells, so when its levels fall, fluid is pulled out of cells, resulting in ascites and peripheral oedema (Kumar and Clark, 2017; Bacon et al, 2005).




People with ascites tend to become symptomatic only if moderate-to-large amounts have accumulated in the abdominal cavity. This can manifest as an increase in abdominal girth with associated discomfort and bloating. As the volume of fluid increases, pressure increases on the diaphragm, causing shortness of breath and a reduction in oxygen saturation. In addition, ascitic fluid can migrate across the diaphragm and accumulate around the lungs (hydrothorax), which can also lead to shortness of breath.


Ascites increases abdominal pressure, which can cause hernias to form; while these can occur anywhere in the abdomen, the most common site is in the umbilicus (umbilical hernia). Surgical repair of hernias in patients with ascites is generally avoided due to the risk of ascites accumulating again and causing pressure on the healing wound, which can lead to ascitic leakage and/or wound breakdown. Surgery is only usually considered if the bowel within the hernia has become twisted. When this happens, the blood supply to the bowel becomes blocked, causing the bowel to become ischaemic; this causes severe pain and can lead to death.


Large amounts of abdominal ascites can impair mobility and make it difficult for patients to sit upright and lie down flat. The excess abdominal fluid can exert pressure on internal organs such as the bladder, causing urinary urgency, or the bowel, which causes constipation.



Ascites can be detected on physical examination through a technique known as percussion. The patient is asked to lie flat on their back – if this can be tolerated – and the health professional taps the abdomen with their fingers (Fig 1). A resonant sound should be heard on percussion over air, but percussion performed over solid organs or fluid will produce a dull sound (Epstein et al, 2008). The tapping should start in the midline and move out towards the flanks. Once a dull sound is heard, the patient should roll onto the opposite side. Gravity will then make any fluid present flow down to the other side of the abdomen (Bickley et al, 2007). The health professional must keep their hand on the abdomen during this process and, once the patient has changed position, tap the exact same site again. A resonant sound should then be heard, as air should have filled the area previously occupied by fluid. This sign is known as ‘shifting dullness’ and is indicative of ascites (Innes et al, 2018; Bickley et al, 2007).


Evidence of ascites can also be provided by imaging. Abdominal ultrasound is the quickest, cheapest and most-convenient method, but computerised tomography (CT) and magnetic resonance imaging (MRI) can be also used, especially for staging disease or following up patients after a cancer diagnosis.


fig 1 abdominal percussion

Ascitic fluid investigations

One method that can help determine the cause of ascites is to measure the amount of protein it contains. Ascites is divided into two subtypes based on the amount of protein contained in the fluid:


  • Exudates – these have a higher protein count and, therefore, appear cloudier;
  • Transudates – these have a lower protein count and, therefore, appear clearer.

Exudates are produced through inflammation and injury; examples of exudate are:


  • Pus – composed of active and dead white blood cells;
  • Catarrhal exudate – present as mucous in the nose or throat.

Transudates are caused by pressure differences between the inside and outside of cells and are associated with conditions such as liver cirrhosis, malnutrition, heart failure and nephrotic syndrome.


In recent years, another way of determining the cause of ascites has emerged and has become the preferred method. It involves taking a blood sample, measuring its albumin level and then subtracting the amount of albumin measured in the ascitic fluid. This metric is called the serum ascites albumin gradient (SAAG) (Hou and Sanyal, 2009); it is calculated as follows:


SAAG = blood serum albumin level − albumin level of ascitic fluid


In the presence of ascites due to portal hypertension caused by conditions such as liver cirrhosis, heart failure and Budd-Chiari syndrome, the SAAG will be >11g/L. In the presence of ascites caused by conditions such as cancer and pancreatitis, it will be <11g/L.




Patients diagnosed with ascites are often prescribed diuretics (often known to patients as water tablets), which help the kidneys remove water and salt. The first-line diuretic of choice is spironolactone, usually started at a dose of 100mg once a day and, if needed, increased at weekly intervals up to a maximum of 400mg daily. If spironolactone alone is not effective, furosemide 40mg can be added to the regimen and its dose increased as long as the patient does not experience any side-effects.


Diuretics can cause disturbances of blood electrolytes such as sodium and potassium, so these must be monitored closely; this is usually done by taking a weekly measurement of urea and electrolytes (UEs). Table 2 shows the levels of sodium and potassium that warrant stopping medication.


Diuretic doses can be titrated up or down, or stopped altogether based on UEs (Table 2) and on weight loss – which means patients must be weighed daily. Drug doses should be adjusted to achieve a weight loss of around 0.5kg/day. In patients with peripheral oedema (fluid in the tissues, normally in the legs) as well as ascites, the aim is to achieve a weight loss of 1kg/day. If weight loss exceeds the target, drug doses need to be reduced (Lawson, 2014).


table 2 adjusting diuretics according to electrolyte counts

Sodium and fluid restriction

Sodium retains fluid, so limiting dietary intake of salt can help prevent extra fluid retention. In patients with cirrhosis who also have ascites, a total dietary sodium intake of 80-120mmol/day is recommended. A negative sodium balance (when sodium intake is less than what the patient excretes) can be achieved in 10-20% of these patients if they do not add any salt to their food and avoid pre-prepared foods (Moore and Aithal, 2006). However, some people may find salt restriction makes food so unpalatable that they have difficulty adhering to such a diet. Referral to a dietitian can be useful for further advice and management.


Fluid restriction should only be considered when ascites is associated with low sodium caused by hypervolaemia (fluid overload). Again, patients may find it difficult to adhere to a fluid-restricted regimen, which has been reported to cause dry mouth and reduce quality of life (Reilly et al, 2015). Nurses can help by offering ice cubes or ice chips to patients, but will need to measure the amount of water these contain to maintain a strict fluid balance. Patients on fluid restriction should be encouraged to maintain good oral hygiene, as this helps keep the mouth fresh.



Patients with moderate-to-large volumes of ascites can be treated by paracentesis (drainage of ascites). A temporary drain is inserted under local anaesthetic and attached to a drainage bag, and the ascitic fluid is left to drain freely over 4-6 hours. The drain tube is held in place by a drain guard dressing that holds the drain against the skin, so it does not need to be sutured. Fig 2 shows the equipment needed for paracentesis. The most common site for ascitic drain insertion is the right or left lower abdominal quadrant, but care must be taken to avoid an enlarged liver or spleen, enlarged abdominal blood vessels, and arteries situated near the umbilicus (Moore and Aithal, 2006).


During ascitic fluid drainage, the patient needs to stay in bed to allow nurses to undertake regular observations; Table 3 outlines how often these should take place. Once the fluid has stopped draining, and the abdomen girth has decreased and is soft to touch, the drain is removed and a waterproof dressing applied to the puncture site.


fig 2 paracentesis equipment

table 3 observations during ascitic fluid drainage

For every 2.5L of ascitic fluid drained, 100ml of 20% albumin is infused intravenously. Albumin is a plasma expander and helps to reduce the risk of a drop in BP. It also helps reduce, in the days following drainage, the risk of acute kidney injury (AKI) linked to the removal of large volumes of ascitic fluid (Kumar and Clark, 2017).


For two days after paracentesis, patients are asked not to take diuretics, again to reduce the risk of AKI. To check kidney function and monitor patients for AKI, UEs need to be measured daily for three or four days after paracentesis. It is important to note that many patients with cirrhosis have low baseline urea and creatinine levels, which means that UE levels can double (indicating kidney injury) while remaining within, or just above, normal levels.


Paracentesis should not be undertaken if platelets are <50 and/or the international normalised ratio (INR) is >2. A low platelet count should be corrected by giving a platelet infusion before paracentesis, while an INR of >2 should be corrected with a transfusion of fresh frozen plasma.


Paracentesis should not be undertaken lightly, as it entails both minor and major risks. Aside from AKI, one of the major risks is haemorrhage because of clotting abnormalities, due to vitamin K deficiency (which can occur in patients who are jaundiced) and/or to clotting factor deficiencies caused by the failing liver. Other serious complications are bowel perforation and introducing infection into the abdomen.


The risk of introducing infection is reduced by removing the drain as soon as clinically indicated; usually the drain is left in place for six hours at the most. Minor risks of paracentesis are discomfort during the procedure and leakage from the puncture site (which may require stitching). Because of the risks, patients need to give written informed consent before the procedure is undertaken.


Spontaneous bacterial peritonitis

Spontaneous bacterial peritonitis (SBP) is an infection of the ascitic fluid, which can occur at any time without warning. Sometimes there are associated symptoms such as fatigue or weakness, deteriorating liver function, abdominal pain, hepatic encephalopathy, fever and shock. However, some patients are asymptomatic.


All patients diagnosed with new-onset ascites should have a sample of ascitic fluid taken and analysed to rule out SBP. (This should also be done to check for other causes of cirrhosis if the cause is uncertain.) Ascitic fluid samples are taken by inserting a needle into the abdomen, aspirating some fluid into a syringe and transferring it into universal containers and blood culture bottles, which are then sent to the laboratory. A white blood cell count of <250mm3 in the ascitic fluid is indicative of SBP (Runyon, 2013).The ascitic fluid is also examined for bacterial growth; if bacteria are found, antibiotic treatment should be initiated.


Patients with SBP used to have a mortality rate of around 90%, but improved diagnosis and treatment mean that the rate has improved to around 20% (EASL, 2010).


Refractory ascites

Sometimes, despite treatment with diuretics, salt restriction and paracentesis, ascites recur. This is called refractory ascites. In some cases, diuretics must be discontinued altogether because of electrolyte disturbances. Sometimes ascites can recur after as little as one week following paracentesis. Patients requiring repeated ascitic fluid drainage should be considered for liver transplantation or transjugular intrahepatic portosystemic shunt (TIPSS) (EASL, 2010; Moore and Aithal, 2006).


Implications for practice

The development of ascites is secondary to many different conditions, and the prognosis and outlook for patients will depend on the underlying cause. Ascites can be managed, but sometimes the underlying problem cannot be resolved. For patients and families, ascites is associated with poorer quality of life and increased risk of infection (especially SBP), renal failure and premature death. As liver cirrhosis tends to occur in younger age groups, it can be particularly difficult for patients and their families to come to terms with symptoms, complications and a shortened life expectancy.


With the development of advanced nursing roles, it is often nurses who: obtain written consent; prescribe local anaesthetic, analgesia and albumin; perform paracentesis; and offer supportive care. Nurses need to draw on their knowledge and skills to deliver high-quality holistic care, and help patients and relatives deal with the complications and poor prognosis of liver cirrhosis. Thoughtful, caring, empathetic support is needed when managing ascites.


Key points

  • Ascites is an abnormal accumulation of fluid in the abdomen
  • The most common cause of ascites is liver cirrhosis
  • Ascites is an indicator that cirrhosis has changed from stable to decompensated
  • Ascites can be treated with diuretics, salt restriction and ascitic fluid drainage (paracentesis)
  • Patients with ascites often struggle with disease prognosis and complications, so empathetic nursing care is needed 

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